Abstract
Systemic immune cell dysfunction is a typical feature of liver diseases and increases the risk of bacterial infection, especially spontaneous bacterial peritonitis. We evaluated functional properties of neutrophil granulocytes in blood and ascites of patients both with and without decompensated cirrhosis. We collected blood and ascites samples from 63 patients with cirrhosis and eight without cirrhosis. Phagocytosis activity (PA) and oxidative burst activity (OBA) were evaluated after ex vivo stimulation with E. coli, while fluorescence signals were measured by flow cytometry. Ascites’ neutrophil function tests were repeated after incubation with autologous plasma. Ascites’ neutrophils showed an impaired PA and OBA (median blood PA 98.1% (86.8–99.8) vs. ascites’ PA 50.5% (0.4–97.3), p < 0.0001; median blood OBA 98.7% (27.5–100) vs. ascites’ OBA 27.5% (0.3–96.7), p < 0.0001). Patients with non-cirrhotic ascites showed higher PA but equally suppressed OBA. Ascites’ neutrophil function could be partially restored after incubation with autologous plasma (median increase PA: 22.5% (−49.7 – +93.2), p = 0.002; OBA: 22.8% (−10.4 – +48.8), p = 0.002). Ascites’ neutrophils of patients with cirrhosis are functionally impaired, but could be partially restored after incubation with plasma. Further investigations are needed to identify the factors in ascites that are associated with neutrophils’ function.
Highlights
Oxidative burst activity in patients with and without SBP
Neutrophil function was determined by flow cytometry after stimulation with inactivated and opsonised E. coli bacteria
It has been suggested that the peritoneal cavity in cirrhosis might be a privileged site with reduced host defence mechanisms[19,20,21,22], there have been limited studies evaluating ascites’ neutrophil function as a potential contributory factor to the specific susceptibility of the peritoneal cavity to bacterial infections
Summary
Oxidative burst activity in patients with and without SBP. The function of the peripheral blood neutrophil counterpart was not studied, so it remains a matter of speculation whether the findings in ascites are a reflection of the systemic neutrophil dysfunction that has been observed in patients with liver failure. Due to this lack, we were interested in whether neutrophils in ascites of patients with decompensated cirrhosis show a higher degree of functional impairment, compared to their blood counterparts, and to ascites’ neutrophils derived from patients with non-cirrhotic ascites
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